Alendronate treatment induces IL-1B expression and apoptosis in glioblastoma cell line

Tricarico, Paola Maura; Epate, Angeladine; Celsi, Fulvio; Crovella, Sérgio

doi:10.1007/s10787-017-0369-5

Cited by 14 publications

(6 citation statements)

References 34 publications

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“…TNF-α and IFN-γ have been shown to synergistically induce apoptosis via the induction of nitric oxide [ 33 ]. Also, IL-1β can induce cell death by apoptosis [ 34 ]. Generally, anti-apoptotic properties that lead to a great neuron survival involve reduction in apoptosis mediators as well as oxidative substances, such as superoxide dismutase and hydrogen peroxide.…”

Section: Resultsmentioning

confidence: 99%

Adenosine Receptors as Neuroinflammation Modulators: Role of A1 Agonists and A2A Antagonists

Navia

Ben

Lambertucci

et al. 2020

Cells

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The pathological condition of neuroinflammation is caused by the activation of the neuroimmune cells astrocytes and microglia. The autacoid adenosine seems to be an important neuromodulator in this condition. Its main receptors involved in the neuroinflammation modulation are A1AR and A2AAR. Evidence suggests that A1AR activation produces a neuroprotective effect and A2AARs block prevents neuroinflammation. The aim of this work is to elucidate the effects of these receptors in neuroinflammation using the partial agonist 2′-dCCPA (2-chloro-N6-cyclopentyl-2′-deoxyadenosine) (C1 KiA1AR = 550 nM, KiA2AAR = 24,800 nM, and KiA3AR = 5560 nM, α = 0.70, EC50A1AR = 832 nM) and the newly synthesized in house compound 8-chloro-9-ethyl-2-phenethoxyadenine (C2 KiA2AAR = 0.75 nM; KiA1AR = 17 nM and KiA3AR = 227 nM, IC50A2AAR = 251 nM unpublished results). The experiments were performed in in vitro and in in vivo models of neuroinflammation. Results showed that C1 was able to prevent the inflammatory effect induced by cytokine cocktail (TNF-α, IL-1β, and IFN-γ) while C2 possess both anti-inflammatory and antioxidant properties, counteracting both neuroinflammation in mixed glial cells and in an animal model of neuroinflammation. In conclusion, C2 is a potential candidate for neuroinflammation therapy.

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Section: Resultsmentioning

confidence: 99%

Adenosine Receptors as Neuroinflammation Modulators: Role of A1 Agonists and A2A Antagonists

Navia

Ben

Lambertucci

et al. 2020

Cells

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“…IL-1β is a crucial gene that helps to regulate inflammatory response, [44] and is involved in cell proliferation, differentiation, and apoptosis. [45] Similarly, TNF-α is an inflammatory cytokine that arises during acute inflammation. It can lead to cell death, but it is also an important factor in fighting cancer or infections.…”

Section: Resultsmentioning

confidence: 99%

Behavior of Neural Cells Post Manufacturing and After Prolonged Encapsulation within Conductive Graphene-Laden Alginate Microfibers

McNamara

Asli²,

Pemathilaka³

et al. 2021

Preprint

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Engineering conductive 3D cell scaffoldings offer unique advantages towards the creation of physiologically relevant platforms with integrated real-time sensing capabilities. Toward this goal, rat dopaminergic neural cells were encapsulated into graphene-laden alginate microfibers using a microfluidic fiber fabrication approach, which is unmatched for creating continuous, highly tunable microfibers. Incorporating graphene increases the conductivity of the alginate microfibers 148%, creating a similar conductivity to native brain tissue. Graphene leads to an increase in the cross-sectional sizes and porosities of the fibers, while reducing the roughness of the fiber surface. The cell encapsulation procedure has an efficiency rate of 50%, and of those cells, approximately 30% remain for the entire 6-day observation period. To understand how encapsulation effects cell genetics, the genes IL-1β, TH, TNF-α, and TUBB-3 are analyzed, both after manufacturing and after encapsulation for six days. The manufacturing process and combination with alginate leads to an upregulation of TH, and the introduction of graphene further increases its levels; however, the inverse trend is true of TUBB-3. Long-term encapsulation shows continued upregulation of TH and of TNF-α, and six-day exposure to graphene leads to the upregulation of TUBB-3 and IL-1β, which indicates increased inflammation.

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“…Recent studies have shown that NLRP3 inflammasome are closely related to the innate immune response of the body. Multiple pathogen-associated molecular patterns and risk-related molecular patterns can activate inflammasome, cause the production of pro-inflammatory cytokines such as IL-1β and provoke apoptosis [16,17]. Emerging studies have shown that NLRP3 inflammasome plays an important role in the development of CI-AKI in vivo and in vitro studies, and mediates downstream apoptosis and inflammatory responses [18,19].It is well known that the mechanism of CI-AKI is closely related to oxidative stress, apoptosis and inflammatory response [20,21].…”

Section: Sift Desk Discussionmentioning

confidence: 99%

Astaxanthin attenuate iohexol-induced human proximal renal tubular epithelial cells injury via the ROS/NLRP3 inflammasome signal pathway

Gao¹,

Yao²,

Sun³

et al. 2019

SDRP-JFST

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Alendronate treatment induces IL-1B expression and apoptosis in glioblastoma cell line

Cited by 14 publications

References 34 publications

Adenosine Receptors as Neuroinflammation Modulators: Role of A1 Agonists and A2A Antagonists

Adenosine Receptors as Neuroinflammation Modulators: Role of A1 Agonists and A2A Antagonists

Behavior of Neural Cells Post Manufacturing and After Prolonged Encapsulation within Conductive Graphene-Laden Alginate Microfibers

Astaxanthin attenuate iohexol-induced human proximal renal tubular epithelial cells injury via the ROS/NLRP3 inflammasome signal pathway

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